This report entails in vivo and in vitro studies concerned with free radical species involved in brain ischemia. The participation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in the early manifestation of cerebral ischemia/reperfusion was investigated in gerbils exposed to transient global ischemia using 4-OH-2,2,6,6-Tetramethylpiperidine-1-oxyl (TPL), a well-known antioxidant. TPL treatment reversed cerebral postischemic hypoperfusion and tissue edema in these animals. The findings are consistent with ROS/RNS participation in tissue injury and the reduction of cerebromicrovascular blood flow (CBF) during postischemic recirculation. The activation/deactivation of signal transduction pathway by oxidation/antioxidation [i.e., using hydrogen peroxide (HO)/TPL] was evaluated in cultured human brain endothelial cells (HBEC) to assess the involvement of endothelial-dependent mechanisms. The data showed that HO activates various 'stress' kinases and vasodilalator-stimulated phosphoprotein (VASP); activation of this pathway was reduced by inhibitors of Rho- or IP-3 kinases, as well as TPL. HO also induced cytoskeleton (actin) rearrangements in HBEC; this effect was prevented by inhibitors of Rho/IP3 kinase or TPL. The observed activation/deactivation of HO-induced 'stress' kinase is in agreement with the reported capacity of ROS/RNS to stimulate the oxidative signal transduction pathway. The noted TPL reduction of HO-induced phosphorylation of kinase strongly suggests that the beneficial effect of TPL implicates the stress signal transduction pathway. This may represent a mechanism for the cerebral postischemic manifestations observed by in vivo experiments.

A growing body of evidence suggests that hyperglycemia-induced oxidative stress plays an important role in diabetic complications, especially Î²-cell dysfunction and failure. Under physiological conditions, reactive oxygen species serve as second messengers that facilitate signal transduction...

Reports on the radical theory of sneezing caused by pollen extracts based on the new research in the U.S. Indication of the result that NADPH oxidases in pollen itself generate a type of free radical known as reactive oxygen species; Demonstration that pollen extracts from weeds, trees and...

Reactive oxygen species (ROS) cause cell damages through protein oxidation leading to pathological processes like cardiovascular disease neurological degeneration and cancer (1). Antioxidants molecules, due to their ability to scavenge and neutralize free radicals, might play a pivotal role in...

Generation of reactive oxygen species (ROS) is a ubiquitous phenomenon in eukaryotic cells' life. Up to the 1990s of the past century, ROS have been solely considered as toxic species resulting in oxidative stress, pathogenesis and aging. However, there is now clear evidence that ROS are not...

Living organisms have evolved ubiquitous mechanisms to manage a vast multitude of Stressors and noxious conditions. Although Nrf2 mainly plays a major role in cellular antioxidant defence, results from recent studies have highlighted its ubiquitous roles in cellular cytoprotection including...

Traditionally, the main focus of the importance of reactive oxygen species (ROS) in oncology is that these species induce DNA damage, leading to a predisposition to cancer. However, it has recently been shown that ROS may have an alternative activity, by modulating tumor cell signaling....